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ID 115707
Author
Ikeda, Mayumi Tokushima University
Kinoshita, Ryo Kumamoto University
Chuang, Victor T.G. Curtin University
Tasaka, Nanami Tokushima University
Matsuo, Nana Tokushima University
Watanabe, Hiroshi Kumamoto University
Otagiri, Masaki Sojo University
Maruyama, Toru Kumamoto University
Keywords
Ultraviolet irradiation
Human serum albumin
Reactive sulfur species
Whitening agent
Oxidative stress
Content Type
Journal Article
Description
Products of ultraviolet (UV) irradiation such as reactive oxygen species (ROS) and nitric oxide (NO) stimulate melanin synthesis. Reactive sulfur species (RSS) have been shown to have strong ROS and NO scavenging effects. However, the instability and low retention of RSS limit their use as inhibitors of melanin synthesis. The free thiol at Cys34 on human serum albumin (HSA) is highly stable, has a long retention and possess a high reactivity for RSS. We report herein on the development of an HSA based RSS delivery system. Sulfane sulfur derivatives released from sodium polysulfides (Na2Sn) react readily with HSA. An assay for estimating the elimination of sulfide from polysulfide showed that almost all of the sulfur released from Na2Sn bound to HSA. The Na2Sn-treated HSA was found to efficiently scavenge ROS and NO produced from chemical reagents. The Na2Sn-treated HSA was also found to inhibit melanin synthesis in B16 melanoma cells and this inhibition was independent of the number of added sulfur atoms. In B16 melanoma cells, the Na2Sn-treated HSA also inhibited the levels of ROS and NO induced by UV radiation. Finally, the Na2Sn-treated HSA inhibited melanin synthesis from L-DOPA and mushroom tyrosinase and suppressed the extent of aggregation of melanin pigments. These data suggest that Na2Sn-treated HSA inhibits tyrosinase activity for melanin synthesis via two pathways; by directly inhibiting ROS signaling and by scavenging NO. These findings indicate that Na2Sn-treated HSA has potential to be an attractive and effective candidate for use as a skin whitening agent.
Journal Title
Redox Biology
ISSN
22132317
Publisher
Elsevier
Volume
14
Start Page
354
End Page
360
Published Date
2017-10-11
Rights
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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DOI (Published Version)
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language
eng
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departments
Pharmaceutical Sciences